Ignet

Gene Information

Gene symbol: NTS

Gene name: neurotensin

HGNC ID: 8038

Related Genes

#	Gene Symbol	Number of hits
1	ADCYAP1	1 hits
2	AGRP	1 hits
3	AGT	1 hits
4	ARC	1 hits
5	CALCA	1 hits
6	CARTPT	1 hits
7	CASP8	1 hits
8	CCK	1 hits
9	CRH	1 hits
10	CYSLTR2	1 hits
11	FOS	1 hits
12	GAL	1 hits
13	GAST	1 hits
14	GCG	1 hits
15	GIP	1 hits
16	GRP	1 hits
17	HBEGF	1 hits
18	HCRT	1 hits
19	HRH1	1 hits
20	IGF2	1 hits
21	INS	1 hits
22	LEP	1 hits
23	MLN	1 hits
24	NMB	1 hits
25	NPY	1 hits
26	NTSR1	1 hits
27	NTSR2	1 hits
28	PMCH	1 hits
29	POMC	1 hits
30	PPY	1 hits
31	PYY	1 hits
32	SST	1 hits
33	STAT3	1 hits
34	TAC1	1 hits
35	TEC	1 hits
36	TNC	1 hits
37	VIP	1 hits
38	VIPR1	1 hits

Related Sentences

#	PMID	Sentence
1	648748	The hyperglycemic response to neurotensin was partially blocked by the histamine H-1 receptor blockers, diphenhydramine and promethazine, and by the H-2 receptor blocker, cimetidine.
2	648748	The effects of histamine on glucose, glucagon, and insulin secretion were similar to those of neurotensin, and the inhibitory effects of both H-1 and H-2 blockers were comparable.
3	648748	The hyperglycemic response to neurotensin was partially blocked by the histamine H-1 receptor blockers, diphenhydramine and promethazine, and by the H-2 receptor blocker, cimetidine.
4	648748	The effects of histamine on glucose, glucagon, and insulin secretion were similar to those of neurotensin, and the inhibitory effects of both H-1 and H-2 blockers were comparable.
5	1381831	We measured hyothalamic NPY and NPY mRNA, along with galanin, neurotensin, and somatostatin in chow-fed rats and in rats with dietary obesity, and examined the effect of dexfenfluramine on these peptides in this model.
6	1381831	Hypothalami were dissected into medial and lateral blocks, and NPY, galanin, neurotensin, and somatostatin were measured by radioimmunoassay.
7	1381831	We measured hyothalamic NPY and NPY mRNA, along with galanin, neurotensin, and somatostatin in chow-fed rats and in rats with dietary obesity, and examined the effect of dexfenfluramine on these peptides in this model.
8	1381831	Hypothalami were dissected into medial and lateral blocks, and NPY, galanin, neurotensin, and somatostatin were measured by radioimmunoassay.
9	1720364	In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls.
10	1720364	The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted.
11	1720364	NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally.
12	1720364	In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls.
13	1720364	The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted.
14	1720364	NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally.
15	1943736	Hypothalamic tissue levels of nine regulatory peptides (bombesin, calcitonin gene-related peptide [CGRP], galanin, neuromedin B, neuropeptide Y [NPY], neurotensin, somatostatin, substance P, and vasoactive intestinal peptide [VIP]) were compared in Aston obese diabetic (ob/ob) and lean (+/?)
16	2227272	All patients had determinations of fasting plasma gastrin, human pancreatic polypeptide, motilin, neurotensin, and somatostatin; 35 had determinations of insulin and gastrin-releasing peptide and 21 had determinations of glucagon.
17	2227272	Motilin was elevated in 29%, human pancreatic polypeptide in 27%, neurotensin in 20%, and gastrin-releasing peptide in 10%, whereas insulin, glucagon, and somatostatin were not elevated in any patient.
18	2227272	Furthermore, no evidence is found to support the conclusions that the detection of the plasma elevation of these peptides is clinically important in assessing MEN-I status, disease extent, or presence of metastatic disease or that elevated levels of motilin, neurotensin, gastrin-releasing peptide, or human pancreatic peptide are associated with any distinct clinical symptoms.
19	2227272	All patients had determinations of fasting plasma gastrin, human pancreatic polypeptide, motilin, neurotensin, and somatostatin; 35 had determinations of insulin and gastrin-releasing peptide and 21 had determinations of glucagon.
20	2227272	Motilin was elevated in 29%, human pancreatic polypeptide in 27%, neurotensin in 20%, and gastrin-releasing peptide in 10%, whereas insulin, glucagon, and somatostatin were not elevated in any patient.
21	2227272	Furthermore, no evidence is found to support the conclusions that the detection of the plasma elevation of these peptides is clinically important in assessing MEN-I status, disease extent, or presence of metastatic disease or that elevated levels of motilin, neurotensin, gastrin-releasing peptide, or human pancreatic peptide are associated with any distinct clinical symptoms.
22	2227272	All patients had determinations of fasting plasma gastrin, human pancreatic polypeptide, motilin, neurotensin, and somatostatin; 35 had determinations of insulin and gastrin-releasing peptide and 21 had determinations of glucagon.
23	2227272	Motilin was elevated in 29%, human pancreatic polypeptide in 27%, neurotensin in 20%, and gastrin-releasing peptide in 10%, whereas insulin, glucagon, and somatostatin were not elevated in any patient.
24	2227272	Furthermore, no evidence is found to support the conclusions that the detection of the plasma elevation of these peptides is clinically important in assessing MEN-I status, disease extent, or presence of metastatic disease or that elevated levels of motilin, neurotensin, gastrin-releasing peptide, or human pancreatic peptide are associated with any distinct clinical symptoms.
25	2428557	Effect of ganglionic blockade on endogenous circulating pancreatic polypeptide, vasoactive intestinal polypeptide, substance P, neurotensin and noradrenaline in healthy controls and long-term insulin-dependent diabetic patients.
26	2428557	Plasma pancreatic polypeptide (PP), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT) and noradrenaline (NA) were measured in eight healthy subjects and 12 long-term insulin-dependent diabetic patients with and without autonomic neuropathy, before and after intravenous infusion of the ganglionic blocking agent trimethaphan camsylate, in order to determine the influence of the autonomic nervous system on the baseline values of the substances.
27	2428557	Effect of ganglionic blockade on endogenous circulating pancreatic polypeptide, vasoactive intestinal polypeptide, substance P, neurotensin and noradrenaline in healthy controls and long-term insulin-dependent diabetic patients.
28	2428557	Plasma pancreatic polypeptide (PP), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT) and noradrenaline (NA) were measured in eight healthy subjects and 12 long-term insulin-dependent diabetic patients with and without autonomic neuropathy, before and after intravenous infusion of the ganglionic blocking agent trimethaphan camsylate, in order to determine the influence of the autonomic nervous system on the baseline values of the substances.
29	2543553	This subgroup also showed lower fasting values of pancreatic polypeptide and motilin were recorded for the obese patients after the fibre-rich period compared to before the study.
30	2543553	Investigations with reference to an entero-hormonal mechanism by measuring neurotensin and peptide YY did not show any variations between the diet periods.
31	2876509	SMS 201-995 (5-100 micrograms) injected subcutaneously in normal and type-2 diabetic subjects 30 min before a test meal caused dose-related suppression of plasma concentrations of insulin, glucagon, and several regulatory gut peptide hormones (gastrin, gastric inhibitory peptide, pancreatic polypeptide, secretin, neurotensin, and motilin).
32	2905691	Reduced hypothalamic somatostatin and neuropeptide Y concentrations in the spontaneously-diabetic Chinese hamster.
33	2905691	In the diabetic hamsters, hypothalamic concentrations of somatostatin and neuropeptide Y were significantly reduced by 25-30% below controls.
34	2905691	None of the other four peptides examined (bombesin, galanin, neurotensin and vasoactive intestinal peptide) differed significantly between the two groups.
35	2905691	Disturbances in neuropeptide Y (the most potent central appetite stimulant yet discovered) and in somatostatin could be related to hyperphagia, an early and possibly primary abnormality of the diabetic syndrome in the Chinese hamster.
36	2908044	Jejunal tissues from 4- to 5-week diabetic rats were examined for their responses to neurokinin (NK) A, NKB, substance P (SP), bradykinin, neurotensin, bethanechol, isoproterenol and phenylephrine.
37	3028898	Whereas the calcium-pentagastrin test provoked a markedly elevated plasma somatostatin level in association with a depressed plasma neurotensin level, the tolbutamide test surprisingly did not.
38	3396814	Mean fasting plasma concentrations of motilin, substance P, and neurotensin from 6 patients did not differ significantly from controls, whereas gastrin and vasoactive intestinal peptide were significantly less than in controls (p less than 0.01).
39	3715064	Basal and postprandial concentrations of immunoreactive neurotensin were measured in insulin dependent diabetic patients and lean and obese noninsulin dependent diabetic patients when partially withdrawn from subcutaneous (s.c.) insulin treatment and again when near normoglycemia had been achieved from insulin infusion by an artificial endocrine pancreas (AEP).
40	3715064	Neither basal nor postprandial neurotensin differed among the 3 groups of diabetic patients during s.c. insulin treatment nor from weight matched nondiabetic subjects.
41	3715064	Basal and postprandial concentrations of immunoreactive neurotensin were measured in insulin dependent diabetic patients and lean and obese noninsulin dependent diabetic patients when partially withdrawn from subcutaneous (s.c.) insulin treatment and again when near normoglycemia had been achieved from insulin infusion by an artificial endocrine pancreas (AEP).
42	3715064	Neither basal nor postprandial neurotensin differed among the 3 groups of diabetic patients during s.c. insulin treatment nor from weight matched nondiabetic subjects.
43	6124374	For instance, cholecystokinin and human pancreatic polypeptide (hPP) may be importantly involved in the regulation of appetite and satiety control and the development of obesity whereas somatostatin, "endorphins", and neurotensin may directly or indirectly modulate islet hormone secretion.
44	6455583	Daily administration of insulin (10-15 IU/kg) to diabetic rats completely reversed this effect, and pancreatic neurotensin levels in these animals returned to control values.
45	7634946	As concerns long-term results, postoperative hormonal status (insulin, neurotensin, cholecystokinin, gastrin) was checked, basal and stimulated with a standardized meal, using standard hormonal assay kits.
46	7912431	A chimeric VIP-PACAP analogue but not VIP pseudopeptides function as VIP receptor antagonists.
47	7912431	In the present study, we have adopted two different approaches used successfully with other peptides in an attempt to identify new VIP receptor antagonists.
48	7912431	The other methodology involves the formation of a COOH-terminal chimeric analogue by combining VIP(6-28) and PACAP(28-38).
49	7912431	Each nonpseudopeptide analogue also inhibited VIP binding with relative potencies of VIP(6-28)-PACAP(28-38) (1 microM) = 2.5 x [4-Cl-D-Phe6,Leu17]VIP, VIP(10-28), neurotensin(6-11)-VIP(7-28) = 6 x [Ac-Tyr1,D-Phe2]GRF.
50	7912431	The reported VIP receptor antagonist, neurotensin(6-11)-VIP(7-28), was also an agonist.
51	7912431	A chimeric VIP-PACAP analogue but not VIP pseudopeptides function as VIP receptor antagonists.
52	7912431	In the present study, we have adopted two different approaches used successfully with other peptides in an attempt to identify new VIP receptor antagonists.
53	7912431	The other methodology involves the formation of a COOH-terminal chimeric analogue by combining VIP(6-28) and PACAP(28-38).
54	7912431	Each nonpseudopeptide analogue also inhibited VIP binding with relative potencies of VIP(6-28)-PACAP(28-38) (1 microM) = 2.5 x [4-Cl-D-Phe6,Leu17]VIP, VIP(10-28), neurotensin(6-11)-VIP(7-28) = 6 x [Ac-Tyr1,D-Phe2]GRF.
55	7912431	The reported VIP receptor antagonist, neurotensin(6-11)-VIP(7-28), was also an agonist.
56	8105515	Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal.
57	8105515	At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known.
58	8105515	Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD.
59	8105515	We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.
60	8105515	Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal.
61	8105515	At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known.
62	8105515	Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD.
63	8105515	We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.
64	8105515	Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal.
65	8105515	At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known.
66	8105515	Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD.
67	8105515	We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.
68	8105515	Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal.
69	8105515	At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known.
70	8105515	Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD.
71	8105515	We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.
72	8324379	We also measured postprandial levels of pancreatic polypeptide and neurotensin as indicators of vagal function and of the delivery of nutrients to the distal small bowel.
73	9625283	The duodenal content of several neuropeptides, namely vasoactive intestinal polypeptide (VIP), neurotensin, neuropeptide Y (NPY), galanin, gastrin-releasing peptide (GRP) and enkephalin was determined by radioimmunoassay of tissue extracts.
74	9625283	There was no statistically significant difference between controls and NOD mice regarding the duodenal content of neurotensin, NPY, galanin or GRP.
75	9625283	The duodenal content of several neuropeptides, namely vasoactive intestinal polypeptide (VIP), neurotensin, neuropeptide Y (NPY), galanin, gastrin-releasing peptide (GRP) and enkephalin was determined by radioimmunoassay of tissue extracts.
76	9625283	There was no statistically significant difference between controls and NOD mice regarding the duodenal content of neurotensin, NPY, galanin or GRP.
77	9792536	Among these, melanin-concentrating hormone (MCH) and neuropeptide Y (NPY) are potent appetite stimulants, whereas alpha-melanocyte-stimulating hormone (alpha-MSH), neurotensin, and glucagon-like peptide (GLP)-1(7-36) amide have appetite-suppressing properties.
78	9792536	In the current study, we describe the functional interactions between orexigenic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin, and GLP-1) peptides after intracerebroventricular (i.c.v.) administration in the rat.
79	9792536	The i.c.v. administration of GLP-1 completely prevents the orexigenic effects of both MCH and NPY.
80	9792536	However, i.c.v. administration of alpha-MSH prevents only the orexigenic effect of MCH, as we have previously shown, but does not prevent the effect of NPY on food intake.
81	9792536	Similarly, i.c.v. administration of neurotensin prevents only the orexigenic effect of MCH, but does not prevent the appetite-stimulating effect of NPY.
82	9792536	Among these, melanin-concentrating hormone (MCH) and neuropeptide Y (NPY) are potent appetite stimulants, whereas alpha-melanocyte-stimulating hormone (alpha-MSH), neurotensin, and glucagon-like peptide (GLP)-1(7-36) amide have appetite-suppressing properties.
83	9792536	In the current study, we describe the functional interactions between orexigenic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin, and GLP-1) peptides after intracerebroventricular (i.c.v.) administration in the rat.
84	9792536	The i.c.v. administration of GLP-1 completely prevents the orexigenic effects of both MCH and NPY.
85	9792536	However, i.c.v. administration of alpha-MSH prevents only the orexigenic effect of MCH, as we have previously shown, but does not prevent the effect of NPY on food intake.
86	9792536	Similarly, i.c.v. administration of neurotensin prevents only the orexigenic effect of MCH, but does not prevent the appetite-stimulating effect of NPY.
87	9792536	Among these, melanin-concentrating hormone (MCH) and neuropeptide Y (NPY) are potent appetite stimulants, whereas alpha-melanocyte-stimulating hormone (alpha-MSH), neurotensin, and glucagon-like peptide (GLP)-1(7-36) amide have appetite-suppressing properties.
88	9792536	In the current study, we describe the functional interactions between orexigenic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin, and GLP-1) peptides after intracerebroventricular (i.c.v.) administration in the rat.
89	9792536	The i.c.v. administration of GLP-1 completely prevents the orexigenic effects of both MCH and NPY.
90	9792536	However, i.c.v. administration of alpha-MSH prevents only the orexigenic effect of MCH, as we have previously shown, but does not prevent the effect of NPY on food intake.
91	9792536	Similarly, i.c.v. administration of neurotensin prevents only the orexigenic effect of MCH, but does not prevent the appetite-stimulating effect of NPY.
92	9876242	Thymic epithelium, including nurse cells (TEC/TNC), as well as other thymic stromal cells (macrophages and dentritic cells), express a repertoire of polypeptide belonging to various neuroendocrine protein families (such as the neurophypophysial, tachykinin, neurotensin and insulin families).
93	9876242	Oxytocin (OT) is more expressed in the TEC/TNC than vasopressin (VP); insulin-like growth factor 2 (IGF-2) thymic expression predominates over IGF-1, and much more over (pro)insulin.
94	9876242	Thus, OT was proposed to be the self antigen of the neurohypophysial family, and IGF-2 the self antigen precursor of the insulin family.
95	9876242	Using an animal model of autoimmune type 1 diabetes (BB rat), we have shown a defect in intrathymic expression of the self antigen of the insulin family (IGF-2) and in IGF-2-mediated T-cell education to recognize and tolerate the insulin family.
96	9934817	The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin.
97	9934817	In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls.
98	9934817	There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content.
99	9934817	There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin.
100	9934817	In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls.
101	9934817	The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin.
102	9934817	In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls.
103	9934817	There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content.
104	9934817	There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin.
105	9934817	In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls.
106	9934817	The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin.
107	9934817	In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls.
108	9934817	There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content.
109	9934817	There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin.
110	9934817	In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls.
111	10509878	The neuroendocrine peptides investigated were peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), neurotensin, and galanin.
112	10509878	In the antrum, VIP, NPY, and galanin concentrations were all significantly lower in prediabetic and diabetic NOD mice than in controls.
113	10509878	In the colon, the concentrations of PYY, somatostatin, VIP, NPY, and galanin were lower in prediabetic and diabetic NOD mice than in controls.
114	10657511	Neuropeptide Y (NPY), melanin concentrating hormone (MCH), orexins A and B, galanin, and agouti -related peptide (AgRP) all act to stimulate feeding while alpha-melanocyte stimulating hormone (alphaMSH), corticotropin releasing hormone (CRH), cholecystokinin (CCK), cocaine and amphetamine regulated transcript (CART), neurotensin, glucagon-like peptide 1 (GLP 1), and bombesin have anorectic actions.(1) Leptin, expressed in the periphery in white adipose tissue, acts in the CNS to modulate the expression of several of these hypothalamic peptides.(1) This creates a functional link between the adipose tissue and the brain that translates the information on body fat provided by leptin to input into energy balance regulating processes.
115	10657511	In the current review we examine the significant role of the melanocortin system (alphaMSH, agouti and AgRP peptides, and their receptors and mahogany protein) and melanin concentrating hormone in the regulation of energy balance.
116	12147141	Meal size is controlled by a series of short-term hormonal and neural signals that derive from the gastrointestinal tract, such as cholecystokinin whereas others may initiate meals, such as the recently discovered hormone, ghrelin.
117	12147141	Other hormones such as insulin and leptin, together with circulating nutrients, indicate long-term energy stores.
118	12147141	When energy stores are low, production of leptin from adipose tissue, and thus circulating leptin concentrations fall, leading to increased production of hypothalamic neurotransmitters that strongly increase food intake, such as neuropeptide Y (NPY), galanin and agouti-related protein (AGRP) and decreased levels of alpha-melanocyte-stimulating hormone (alpha-MSH), cocaine and amphetamine-regulated transcript (CART) and neurotensin that reduce food intake and increase energy expenditure.
119	12147141	The finding that mutations in leptin and POMC lead to severe early onset obesity in humans has highlighted the importance of these peptides in humans.
120	15862312	We show here that long transcribed but untranslated CGG-repeat tracts are toxic to human cells and alter the expression of a wide variety of different genes including caspase-8, CYFIP, Neurotensin and UBE3A.
121	16505217	Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus.
122	16505217	Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance.
123	16505217	However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons.
124	16505217	The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined.
125	16505217	We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice.
126	16505217	In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons.
127	16505217	Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin.
128	16505217	We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons.
129	16505217	POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system.
130	16505217	Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus.
131	16505217	Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance.
132	16505217	However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons.
133	16505217	The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined.
134	16505217	We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice.
135	16505217	In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons.
136	16505217	Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin.
137	16505217	We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons.
138	16505217	POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system.
139	16505217	Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus.
140	16505217	Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance.
141	16505217	However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons.
142	16505217	The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined.
143	16505217	We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice.
144	16505217	In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons.
145	16505217	Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin.
146	16505217	We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons.
147	16505217	POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system.
148	16505217	Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus.
149	16505217	Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance.
150	16505217	However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons.
151	16505217	The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined.
152	16505217	We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice.
153	16505217	In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons.
154	16505217	Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin.
155	16505217	We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons.
156	16505217	POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system.
157	16682681	The authors examined blood pressure, glucose, insulin, and neurotensin before and after intake of 75 g glucose with or without voglibose in 28 neurologic patients and 20 healthy controls.
158	16682681	Voglibose significantly prevented hypotension and neurotensin increment after glucose intake and had no influence on glucose or insulin increment.
159	16682681	The authors examined blood pressure, glucose, insulin, and neurotensin before and after intake of 75 g glucose with or without voglibose in 28 neurologic patients and 20 healthy controls.
160	16682681	Voglibose significantly prevented hypotension and neurotensin increment after glucose intake and had no influence on glucose or insulin increment.
161	17118789	Characterization of monoclonal antibodies directed against the rat neurotensin receptor NTS1.
162	17192574	Some self-antigens (oxytocin, neurotensin, insulin-like growth factor 2 [IGF-2]) have been selected to be predominantly expressed in thymic epithelium and to be presented to thymus T cells for educating them to tolerate other antigens related to them.
163	17192574	In the insulin family, IGF2 is dominantly transcribed in cortical (c) and medullary (m) thymic epithelial cells (TECs), whereas the insulin gene (INS) is expressed at low level by only a few subsets of mTECs.
164	17192574	Intrathymic transcription of both IGF2 and INS is under the control of the autoimmune regulator (Aire) gene.
165	17192574	The highest concentrations of IGF-2 in the thymus explain why this peptide is much more tolerated than insulin, and why tolerance to IGF-2 is so difficult to break by active immunization.
166	17192574	The high level of tolerance to IGF-2 is correlated to the development of a tolerogenic/regulatory profile when the sequence B11-25 of IGF-2 (homologous to the autoantigen insulin B9-23) is presented to DQ8+ type 1 diabetic patients.
167	17192574	Since subcutaneous and oral insulin does not exert any tolerogenic properties, IGF-2 and other thymus self-antigens related to type 1 diabetes (T1D) should be preferred to insulin for the design of novel specific antigen-based preventive approaches against T1D.
168	19679549	Recently, we identified a novel crosstalk between insulin and G protein-coupled receptor (GPCR) signaling pathways in human pancreatic cancer cells.
169	19679549	Insulin enhanced GPCR signaling through a rapamycin-sensitive mTOR-dependent pathway.
170	19679549	Here, we determined whether metformin disrupts the crosstalk between insulin receptor and GPCR signaling in pancreatic cancer cells.
171	19679549	Treatment of human pancreatic cancer cells (PANC-1, MIAPaCa-2, and BxPC-3) with insulin (10 ng/mL) for 5 minutes markedly enhanced the increase in intracellular [Ca(2+)] induced by GPCR agonists (e.g., neurotensin, bradykinin, and angiotensin II).
172	19679549	Metformin pretreatment completely abrogated insulin-induced potentiation of Ca(2+) signaling but did not interfere with the effect of GPCR agonists alone.
173	19679549	Insulin also enhanced GPCR agonist-induced growth, measured by DNA synthesis, and the number of cells cultured in adherent or nonadherent conditions.
174	19679549	Low doses of metformin (0.1-0.5 mmol/L) blocked the stimulation of DNA synthesis, and the anchorage-dependent and anchorage-independent growth induced by insulin and GPCR agonists.
175	20631047	Recently, glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) have received much attention regarding possible roles in aetiology and treatment of type 2 diabetes.
176	20631047	Xenin also exerted an additive effect on GIP, GLP1 and neurotensin-mediated insulin secretion.
177	21907138	Leptin action via neurotensin neurons controls orexin, the mesolimbic dopamine system and energy balance.
178	21907138	Thus, LHA LepRb(Nts) neurons mediate physiologic leptin action on OX neurons and the mesolimbic DA system, and contribute importantly to the control of energy balance.
179	22522617	Xenin-25 amplifies GIP-mediated insulin secretion in humans with normal and impaired glucose tolerance but not type 2 diabetes.
180	22522617	Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS).
181	22522617	Xenin-25 is a 25-amino acid neurotensin-related peptide that amplifies GIP-mediated GSIS in hyperglycemic mice.
182	22522617	Although magnitudes of insulin secretory responses to GIP were similar in all groups, ISRs were not restored to normal in subjects with IGT and T2DM.
183	23064014	A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin.
184	23064014	Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin.
185	23064014	The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared.
186	23064014	It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity.
187	23064014	A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin.
188	23064014	Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin.
189	23064014	The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared.
190	23064014	It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity.
191	23064014	A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin.
192	23064014	Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin.
193	23064014	The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared.
194	23064014	It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity.
195	23064014	A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin.
196	23064014	Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin.
197	23064014	The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared.
198	23064014	It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity.
199	23696845	Transient and stable expression of the neurotensin receptor NTS1: a comparison of the baculovirus-insect cell and the T-REx-293 expression systems.
200	23696845	Here we constructed a suspension T-REx-293 cell line to stably express an engineered neurotensin receptor 1 (NTS1) mutant and we quantitatively compared this cell line with the transient baculovirus-insect cell system throughout a milligram-scale NTS1 expression and purification process.
201	23696845	This work demonstrates two approaches for preparing milligram quantities of purified NTS1 suitable for structural studies and provides useful input to users in choosing and optimizing an appropriate expression host for other GPCRs.
202	23696845	Transient and stable expression of the neurotensin receptor NTS1: a comparison of the baculovirus-insect cell and the T-REx-293 expression systems.
203	23696845	Here we constructed a suspension T-REx-293 cell line to stably express an engineered neurotensin receptor 1 (NTS1) mutant and we quantitatively compared this cell line with the transient baculovirus-insect cell system throughout a milligram-scale NTS1 expression and purification process.
204	23696845	This work demonstrates two approaches for preparing milligram quantities of purified NTS1 suitable for structural studies and provides useful input to users in choosing and optimizing an appropriate expression host for other GPCRs.
205	23696845	Transient and stable expression of the neurotensin receptor NTS1: a comparison of the baculovirus-insect cell and the T-REx-293 expression systems.
206	23696845	Here we constructed a suspension T-REx-293 cell line to stably express an engineered neurotensin receptor 1 (NTS1) mutant and we quantitatively compared this cell line with the transient baculovirus-insect cell system throughout a milligram-scale NTS1 expression and purification process.
207	23696845	This work demonstrates two approaches for preparing milligram quantities of purified NTS1 suitable for structural studies and provides useful input to users in choosing and optimizing an appropriate expression host for other GPCRs.